It’s important to keep a high index of suspicion when worrying about Compartment Syndrome; keep the 6 P’s in mind. It’s also important to know how to assemble and use a compartment measurement kit if you’re searching for hard, objective data.

1.) contents of the pressure measurement kit
2.) remove contents from wrapping
3.) attach chamber to the pre-filled saline syringe
4.) place the aforementioned into the monitor/unit
5.) place needle onto chamber
6.) eject excess air, if present, from syringe
7.) zero the assembled unit at the angle you will be entering compartment
8.) insert, inject 2-3 drops of saline, and await measurement

When interpreting a compartment’s pressure, there’s the old way, and the new way:

If a patient’s CD4 count is unknown, the Absolute Lymphocyte Count (ALC) can act as a temporary surrogate.

ALC= WBC x % of Lymphocytes.

Here’s a quick review of the literature:

One of the more highly quoted studies states a CD4 count of <200 × 10(6) cells/μL is very likely if the ED ALC is <950 × 10(6) cells/μL and less likely if the ALC is >1,700 × 10(6) cells/μL, Napoli et al (2011).

Two studies performed in non-ED setting showed a good correlation between the CD4 count and ALC. There is some question as to whether these results are applicable or generalizable to the ED population, since all of the participants were tested during routine examinations, not while they were acutely ill, Blatt et al (1993) and Fournier AM et al (1993).

While a single ALC threshold was neither sensitive nor specific for a low CD4 count, the investigators determined two valuable cut-offs of 1000 and 2000 cells/mm3.

– An ALC less than 1000 cells/mm3 was 91% predictive in identifying patients with CD4 counts less than 200 cells/mm3 (sensitivity only 67%, but specificity 96%).– An ALC greater than 2000 cells/mm3 was 95% predictive in identifying CD4 counts greater than 200 cells/mm3.
The authors concluded that patients with ALCs greater than 2000 cells/mm3 might be less susceptible to opportunistic infections, while those with ALCs less than 1000 cells/mm3 are at higher risk. These researchers had no access to clinical data and couldn’t account for factors such as antiretroviral therapy or the presence of acute infection such as sepsis, pneumonia, or TB.

There are of course other studies which show the ALC isn’t greatPirzada et al (2006), and others where it is decent.

These analyses of the ALC could proof useful in many resource poor areas of the world with rising rates of HIV/AIDS as shown by these studies in India and Africa, for example.

Some more on Perfusion Physiology:
-25% goes of the circulating volumes goes to the placenta.
-During cardiac arrest, displacement of the uterus alleviate IVC compression (see Tilt). However, in this circumstance tilting the patient may impede effective CPR. Instead have an assistant manually displace the uterus while leaving the patient in the supine position.
-Perimortem C-sxn can increase the mother’s cardiac output by up to 80%.

For the ED physician, one of our primary concerns if whether this is something that we can handle or does it require surgical management. We should feel comfortable managing perirectal abscesses but the collections in other anorectal areas such as the intersphincteric, ischiorectal and supralevator spaces require surgical management.

The most feared complication is fistula formation which can form in anywhere between 30 – 60% of anorectal abscesses. If you are going to perform an I&D of an anorectal abscess in the ED, taking a culture is of utmost importance. If the culture is growing common GI flora (Bacteroides, E. coli, Enterobacterstaph) you should be suspicious for an underlying fistula while you can feel more comfortable if your culture comes back with staph or strep as this is likely your run of the mill abscess. Incision and drainage is the definitive treatment but you should consider antibiotics if they patient displays systemic symptoms, is a diabetic or is immunosuppressed.

When faced with a newborn patient with elevated bilirubin levels:
1.) Remember the Bhutani Nomogram.
2.) Get your patient under phototherapy as soon as possible.
3.) Appropriate follow up is imperative.

A 65 yo M pt with PMH of ESRD, HTN, CAD comes in c/o SOB x3 days after missing hemodialysis twice in the past week. A portable CXR is ordered, and it looks similar to this:http://radiopaedia.org/cases/apo-arrowsjpg

MEGACASE: 75 yo F with history of ESRD on HD presents to your E.D. after a looooong bus ride with unilateral leg swelling, shortness of breath, hemoptysis, and a recent history of hip surgery. Your thorough history further reveals that the patient has asthma, a severe shellfish allergy, and has had contrast reactions in the past. To make matters worse, the patient is writhing in pain on the stretcher complaining of right flank pain radiating to the groin and a history of renal calculus last year. And for some reason, this patient is still finding the time to tell you she has a “sore throat,” with fever, cough, tonsillar exudate and cervical lymphadenopathy. Oh yeah, and her throat snaps shut like a bear-trap if she has penicillin.

There may be a slightly increased risk of pulmonary edema with iodinated contrast secondary to higher molecular weights, but most hospitals use non-iodinated contrast now. Patients may continue their current dialysis schedule so long as they are dialysed within 24-72 hrs post-contrast administration, regardless of anuric/oliguric status. Check out wha t the American College of Radiology says:
“… Unless an unusually large volume of contrast medium is administered or there is substantial underlying cardiac dysfunction, there is no need for urgent dialysis after intravascular iodinated contrast medium administration.” ACR, version 9, pg 26. (http://www.acr.org/quality-safety/resources/contrast-manual)

“The efficacy of corticosteroid and/or antihistamine prophylaxis is unknown, though some have suggested this practice. However, given the likely differing mechanisms between acute and delayed reactions, as well as the extreme rarity or nonexistence of severe delayed reactions, premedication prior to future contrast-enhanced studies is not specifically advocated in patients with solely a prior history of mild delayed cutaneous reaction.” ACR, version 9, page 40. (http://www.acr.org/quality-safety/resources/contrast-manual)

4.) I’ve heard pen allergic patient’s should never, ever get cephalosporins because the rate of cross-reactivity is 10%. This has to be true.

Listen, pal…

Well, when penicillins and cephalosporins were first produced, the were often made in the same factories – this 10% figure is more likely related to cross-contamination during the production process, not cross-reactivity. The actual rate is closer to 1-3%. There may be higher rates with 1st or 2nd generation cephalosporins, but 3rd generation or higher seem to be fine. Furthermore, the proportion of patients claiming to have a PCN allergy, that actually have a true PCN allergy, is 3%. Overall, the rate of anaphylaxis to cephalosporin in patient’s with a history of anaphylaxis to PCN in 0.001%.

5.) I know antibiotics can’t prevent PSGN. I get it, I know. But what about for Acute Rheumatic Fever (ARF)?

This one’s gotta be right.
As it turns out: not really. The rate of ARF is so low in industrialized nations, that the CDC does not track incidence of the disease any more. (In aboriginal populations, older thinking still holds strong; ARF remains problematic and necessitates antibiotic therapy). The risk of sequela from the disease is significantly and statistically low, and it is a self-limiting process. A Cochrane review demonstrated “resolution and improvement of pain in participants with sore throat” when comparing the efficacies of steroids and antibiotics. (http://www.ncbi.nlm.nih.gov/m/pubmed/23076943/)